This is a disease peculiar to the Pacific Northwest. In consequence of this fact it is often called Pacific Coast canker and Northwestern apple-tree anthracnose. It is known to occur most abundantly in the states of Washington and Oregon. It is not recorded in California, although it probably is present in the northern part of that state. It was once reported as far east as Nebraska, but the disease is unknown in any section of the United States other than that already indicated. Outside of the United States it is found only in British Columbia. It is believed that the apple-tree anthracnose originated somewhere within its present geographical range on some native host. It did not begin to attract serious attention on the apple, however, until 1891. Since that time its ravages have increased until in the Northwest the anthracnose is second in importance only to apple scab. It is most serious in those regions west of the Cascade Mountains, where considerable rainfall occurs. It is rarely serious in eastern Oregon.

On account of the nature of the injury the amount of the losses is difficult to estimate. The twigs, sometimes the larger branches, and even the trunks of young trees are likely to be girdled. A single tree may show from one to more than one hundred cankers varying in length from one - fourth to six inches or even larger. Affected branches are weakened and often are broken by a heavy load of fruit. Stored fruit and even fruits still in the orchard are rotted by the anthracnose pathogene.

Symptoms

The disease is known by the cankers which are produced on the woody parts (Fig. 23). These are characteristically dark, sunken, dead areas in the bark. On this account the disease has been called Black Spot canker, black canker and dead spot. Cankers are found most abundantly on the younger branches; that is, those having a diameter of two to three inches or less; but larger limbs and trunks are not always free from such lesions. On older branches the cankers are often more or less superficial, not extending to the wood. But ordinarily on younger limbs the bark and cambium are dead and the sap - wood is discolored to a limited extent.

The first evidences of this canker appear ordinarily from November to January, depending on the season. The most numerous and the most destructive cankers appear in November and December. When first evident, the lesion is circular, less than an inch in diameter, and the surface is not sunken. In this stage the bark is discolored beneath the surface and has a water - soaked appearance. Soon the discoloration extends to the cambium and here it spreads out, often being more extensive than the surface discoloration would indicate. The canker develops very little through the winter, but in March and April it enlarges rapidly. As it enlarges its shape becomes ellipsoidal,.and the surface sinks slowly. Sometimes the bark shows concentric zones of slightly varying color. The margin of the canker in the later stages of its development is limited by a crevice, which is finally bounded by a callus.

Toward the middle of the summer small, conical elevations are observed on the canker. These burst through the bark in a triangular or transverse manner, exposing a creamy mass the fruiting structures of the pathogene. By late summer or fall the canker may have attained a depth of one-half an inch, a length of ten inches, and a breadth of three to four inches. Sometimes two or more cankers become confluent and thus larger lesions are produced. In older cankers, the bark may drop out leaving a wound, although this may not take place before the canker is three years old. The smaller cankers sometimes heal slowly by callus - formation. In other cases the wound never heals, but instead the limb is completely girdled.

The disease is not uncommon on the fruit, either in the orchard or in storage. The lesions may begin anywhere on the surface; frequently they center about one end, or about an injury of some sort. The apple - limbs.

Fig. 23 Northwestern anthracnose cankers

Fig. 23. - Northwestern anthracnose cankers on flesh of the diseased portion becomes light - brown, the surface depressed, and the texture dry and leathery. Within the affected area the fruiting pustules of the pathogene develop in concentric circles; finally they split open, exposing the creamy substance as described for the canker.

No variety is wholly immune to the disease and some are nearly ruined by it. While it would appear that certain varieties are generally more susceptible than others, the degree of susceptibility varies considerably in different orchards of the same variety, and in different trees of the same variety in any given orchard. The evidence indicates that the kind of soil has little to do with susceptibility. Some hold that the Baldwin, Spitzenberg and Jonathan are most commonly attacked, and that the Newtown, Rhode Island and Graven stein are somewhat less susceptible. Those showing less tendency to be affected are the Ben Davis, Northern Spy, Winesap, Tompkins King and Hubbardston.

Cause Of Anthracnose

The apple-tree anthracnose is caused by the fungus Neofabrcea Malicorticis. In its structure and habits it is very similar to the fungus Pseudopeziza Ribis Kleb., which causes the currant anthracnose. It spends the winter as almost inactive mycelium in the cankers. In the spring the fungus renews activities for a short period, but usually stops its further spread as soon as the cambium becomes active. In midsummer those cankers which were initiated the previous fall form acervuli (Fig. 23, extreme left). With the advent of the autumn rains the acervuli become active, the conidia oozing forth in a creamy, gelatinous mass. On being dried by the wind the conidia are carried to other limbs and to fruits. With the return of the rains the conidial masses again ooze out, and the process of dissemination is repeated. In many cases conidia are doubtless washed by the rain to points below the cankers. In general the conditions prevailing from October to December are very favorable to spore-germination. The fungus is capable of entering its host through wounds in the bark and fruit; however, these wounds are not necessary to penetration. The uninjured bark is penetrated in most cases, chiefly through the lenticels. The healthy, uninjured skins of fruits may be penetrated directly. The fungus in the fruits produces the rot already described, but such fruits apparently never play any further part in assisting the fungus to complete its life-cycle. The fungus undoubtedly perishes with the destruction of the affected fruit. In the limbs, however, the fungus develops advantageously. It grows slowly after entrance into the bark, killing the bark-cells as it progresses. The cambium, sapwood, and even the heart - wood are also affected beneath the canker, but there is no evidence that new cankers arise by growth of the mycelium to points above or below such lesions. As previously pointed out, the fungus develops very slowly during the winter. The following March and April growth is resumed; growth ceases, however, with the initial spring activities of the cambium. By midsummer, the acervuli are produced, and the first year's cycle is completed.

In the fall, two years after infection, the sexual stage of the fungus develops in the old cankers (Fig. 23, center). The fruiting bodies formed are apothecia. They arise in the clefts in the bark formed by the old acervuli, developing in the mycelial cushions left by these asexual structures. Under the moist conditions of the autumn the apothecia become swollen; if dry weather prevails for a time, they seem to disappear, and then to reappear with the return of the next wet weather. If favorable conditions prevail for any length of time, the asci elongate, swell, and the ascospores are finally ejected forcibly. These spores are carried by the wind to the susceptible organs of the apple, where infection results as described for the conidia.

It is to be noted that the conidia may continue to develop in a canker for at least three years. Thus cankers from one to three years old are sources of trouble. Furthermore, diseased bark which falls to the ground may develop the ascospores as described above. And finally, the inocula (conidia and ascospores) may come not only from the apple-tree but from the pear, on which fruit - tree the fungus also occurs.

Control

In applying remedial measures it should be borne in mind that: (1) while the disease appears to be most serious on certain varieties, no variety is wholly immune; (2) the disease is caused by a fungus; (3) the causal fungus infects the trees in the fall, particularly from October to December; (4) the fungus can enter through wounds, lenticels or unbroken surfaces; (5) cankers produced on the limbs are the only source of the inocula - these give rise to all the trouble; (6) these cankers are a dangerous source even when three years old; (7) fallen bark from one-year - old cankers is also a source of the inoculum; (8) the fungus inhabits not only the apple, but also the pear, which may be a source of trouble.

It is therefore out of the question at present to rely on any variety to resist the attacks of the fungus. Any spraying which is done must be accomplished before the most important period of inoculation and infection. It has been shown that old orchards may be cleaned by proper spraying. Bordeaux mixture 6-6-50 is said to be better than lime sulfur for this purpose. For this disease spray as follows: (1) as soon as possible after the fruit is picked; (2) again within two or three weeks. Where the trouble is serious an application should be made at least once before the fruit is picked; this may be made about September 15, or before the first autumn rains. Then spray twice as directed above. These applications should thoroughly coat the limbs to protect them from the attacks of the fungus. Cankers on the more valuable limbs of younger trees may be removed, in which case the debris should be destroyed and the wound coated with coal - tar. The removal and destruction of certain limbs may at times prove helpful. For example, a limb bearing several cankers ought to be so treated. Surgical and pruning measures should in any case be only supplementary to spraying. It should be remembered that the wholesale removal of cankers from large trees where hundreds of lesions occur is an expensive and a laborious method.

References

Jackson, H. S. Apple tree anthracnose. Oregon Crop Pest and Hort.

Bienn. Rept. 1911-1912: 178 - 197. 1913. Cordley, A. B. Apple tree anthracnose, a new fungous disease.

Oregon Agr. Exp. Sta. Bul. 60: 3 - 8. 1900. . Lawrence, W. H. Black spot canker. Washington Agr. Exp. Sta.

Bul. 66: 4 - 35. 1904. Jackson, H. S. Apple tree anthracnose. Oregon Agr. Exp. Sta. Circ.

17:2 - 4. 1911. Cordley, A. B. Some observations on apple tree anthracnose. Bot.

Gaz. 30: 48-58. 1900. Piper, C. V. Orchard enemies of the Pacific northwest. Blackspot apple canker. U. S. Agr. Dept. Farmers' Bul. 153: 31 - 33. 1902.